Affiliation:
1. Laboratorium Badań Molekularnych, Akademia Wychowania Fizycznego im. Jerzego Kukuczki w Katowicach
Abstract
Recently, the crosstalk between autophagy and apoptosis has attracted broader attention. Basal autophagy serves to maintain cell homeostasis, while the upregulation of this process is an element of stress response that enables the cell to survive under adverse conditions. Autophagy may also determine the fate of the cell through its interactions with cell death pathways. The protein networks that control the initiation and the execution phase of these two processes are highly interconnected. Several scenarios for the crosstalk between autophagy and apoptosis exist. In most cases, the activation of autophagy represents an attempt of the cell to cope with stress, and protects the cell from apoptosis or delays its initiation. Generally, the simultaneous activation of pro-survival and pro-death pathways is prevented by the mutual inhibitory crosstalk between autophagy and apoptosis. But in some circumstances, autophagy or the proteins of the core autophagic machinery may promote cellular demise through excessive self-digestion (so-called “autophagic cell death”) or by stimulating
the activation of other cell death pathways. It is controversial whether cells actually die via
autophagy, which is why the term “autophagic cell death” has been under intense debate lately.
This review summarizes the recent findings on the multilevel crosstalk between autophagy
and apoptosis in aspects of common regulators, mutual inhibition of these processes, the stimulation
of apoptosis by autophagy or autophagic proteins and finally the role of autophagy
as a death-execution mechanism.
Subject
Infectious Diseases,Microbiology (medical)
Cited by
67 articles.
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